Cellular Mechanisms and Therapeutic Potentials of Neurodevelopmental Defects

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Neuroscience".

Deadline for manuscript submissions: 31 May 2026 | Viewed by 926

Special Issue Editors


E-Mail Website
Guest Editor
Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy
Interests: down syndrome; pathological mechanism of brain development; molecular mechanisms of neurodegeneration; therapeutic approaches for neurodevelopmental defects and neurodegeneration; physiological and pathological activity of neural networks involved in memory and learning functions
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department for Life Quality Studies, University of Bologna, Rimini, Italy
Interests: down syndrome; physiological and pathological molecular mechanisms underlying brain development; therapeutic ap-proaches for neurodevelopmental defects; synaptic plasticity in physiological and pathological conditions
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Biomedical and Neuromotor Sciences, University of Bologna, 40126 Bologna, Italy
Interests: brain development; neurogenesis; neurodevelopmental disease; dendritic spine; synapses; synaptic plasticity; learning and memory
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department for Life Quality Studies, University of Bologna, Rimini, Italy
Interests: down syndrome; physiological and pathological molecular mechanisms underlying brain development; therapeutic ap-proaches for neurodevelopmental defects; synaptic plasticity in physiological and pathological conditions
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodevelopmental disorders arise from genetic and environmental perturbations that disrupt the finely tuned processes of brain development, including neuronal proliferation, migration, differentiation, and synaptic maturation. Recent advances in genomics, cellular neuroscience, and imaging have greatly expanded our understanding of the molecular and cellular cascades governing brain development, revealing convergent mechanisms across apparently distinct conditions such as intellectual disability, autism spectrum disorder, epilepsy, and rare monogenic syndromes. This Special Issue, entitled “Cellular Mechanisms and Therapeutic Potentials of Neurodevelopmental Defects”, aims to present original research and reviews that dissect how alterations in key cellular pathways—such as those controlling synaptic plasticity, neurogenesis, glial function, and neuronal connectivity—contribute to the onset and progression of developmental brain dysfunction. Particular emphasis will be placed on studies employing cutting-edge experimental models, as well as those exploring innovative therapeutic strategies. By integrating mechanistic insights with translational perspectives, this collection seeks to advance our understanding of neurodevelopmental pathology in order to foster the development of targeted, mechanism-based interventions for these complex and often lifelong disorders.

Dr. Sandra Guidi
Dr. Fiorenza Stagni
Dr. Beatrice Uguagliati
Dr. Marco Emili
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neurodevelopmental disorders
  • neuronal connectivity
  • precocious therapies
  • synaptic plasticity
  • neurogenesis
  • glial function

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

15 pages, 1355 KB  
Article
Early Postnatal Ethanol Exposure Has Long-Term Behavioral Consequences in Female Mice
by Elizabeth C. Plunk, MaKenna Y. Cealie, James C. Douglas, Paul D. Drew and Ania K. Majewska
Cells 2026, 15(7), 608; https://doi.org/10.3390/cells15070608 - 30 Mar 2026
Viewed by 634
Abstract
Background/Objectives: Fetal alcohol spectrum disorders (FASDs) occur in nearly 5% of children in the United States and have been associated with alterations in neurological functions, neuroanatomical changes, and behavioral deficits encompassing an individual’s lifetime. Alterations in myelination have been reported in both [...] Read more.
Background/Objectives: Fetal alcohol spectrum disorders (FASDs) occur in nearly 5% of children in the United States and have been associated with alterations in neurological functions, neuroanatomical changes, and behavioral deficits encompassing an individual’s lifetime. Alterations in myelination have been reported in both rodent models and humans. The cerebellum is a heavily myelinated brain region, and oligodendrocyte and myelination transcripts have been reported to be altered in the cerebellum following early-life ethanol (EtOH) exposure in a mouse model. In this study, we investigated cerebellar-recruited behaviors in adult female mice that were exposed to EtOH from postnatal day (P) 4 to P9. We investigated whether changes in oligodendrocyte lineage markers were present in adulthood. Methods: C57BL/6J offspring received a total of 5.0 g/kg/day of either ethanol (EtOH) or saline in two separate doses delivered subcutaneously two hours apart from P4 to P9. On P21, offspring were weaned and housed with same-sex littermates throughout the duration of the study. From P60 to P90, females underwent behavioral testing including an open field test (OFT), rotarod, and balance beam. Behavior naïve littermates were euthanized on P105, and cerebella were collected for qPCR to assess oligodendrocyte lineage transcripts. Results: We reported that, following EtOH exposure from P4 to P9, adult female mice had increased ambulatory behaviors in the OFT and subtle changes in behavior in the rotarod and balance beam compared to saline-exposed controls. Despite the behavioral changes observed in adulthood, we found that alterations in oligodendrocyte lineage transcripts present on P10 did not persist into adulthood. Conclusions: Subcutaneous injection of EtOH from P4 to P9 resulted in long-term consequences in locomotor and cerebellar-recruited behaviors in female mice. Full article
Show Figures

Figure 1

Back to TopTop